From genotype to phenotype: adaptations of Pseudomonas aeruginosa to the cystic fibrosis environment

Abstract

Pseudomonas aeruginosa is one of the main microbial species colonizing the lungs of cystic fibrosis patients and is responsible for the decline in respiratory function. Despite the hostile pulmonary environment, P. aeruginosa is able to establish chronic infections thanks to its strong adaptive capacity. Various longitudinal studies have attempted to compare the strains of early infection with the adapted strains of chronic infection. Thanks to new '-omics' techniques, convergent genetic mutations, as well as transcriptomic and proteomic dysregulations have been identified. As a consequence of this evolution, the adapted strains of P. aeruginosa have particular phenotypes that promote persistent infection.

Keywords: Pseudomonas aeruginosa; adaptation; cystic fibrosis; genomic; phenotype.

Fig. 1.

Number of longitudinal studies identifying stop (red), frameshifts (yellow) or missense (grey) mutations in 48 genes. Non-synonymously mutated genes and corresponding types of mutations were recovered from the longitudinal studies listed in Table 1. Genes in bold were affected by mutations predicted to have a drastic impact on protein function [17] or induce a partial or total loss-of-function [6].

Fig. 2.

Pathways related to metabolism (a), antimicrobial resistance (b), virulence (c) and biofilm formation (d) altered during P. aeruginosa adaptation to the CF environment. DNA sequences of products in bold have been shown to accumulate non-synonymous mutations. Intergenic regions surrounding products that are underscored are mutated. Late isolates present a convergent transcriptomic dysregulation of the products marked by asterisks in comparison to early isolates.